scholarly journals In Vitro-Derived “Neural Stem Cells” Function as Neural Progenitors Without the Capacity for Self-Renewal

Stem Cells ◽  
2006 ◽  
Vol 24 (3) ◽  
pp. 731-738 ◽  
Author(s):  
Gregory P. Marshall ◽  
Eric D. Laywell ◽  
Tong Zheng ◽  
Dennis A. Steindler ◽  
Edward W. Scott
2010 ◽  
Vol 476 (2) ◽  
pp. 74-78 ◽  
Author(s):  
Yang Wang ◽  
Yunqian Guan ◽  
Fang Wang ◽  
Aihua Huang ◽  
Shuyan Wang ◽  
...  

PLoS ONE ◽  
2020 ◽  
Vol 15 (12) ◽  
pp. e0243644
Author(s):  
Yunfeng Jiang ◽  
Yue Wang ◽  
Yu Sun ◽  
Hong Jiang

Background Exposure to anesthetics during brain development may impair neurological function, however, the mechanisms underlying anesthetic neurotoxicity are unclear. Recent studies indicate that long non-coding RNAs (lncRNAs) are crucial for regulating the functional brain development during neurogenesis. This study aimed to determine the regulatory effects and potential mechanisms of lncRNA Peg13 (Peg13) on sevoflurane exposure-related neurotoxicity against neural stem cells (NSCs). Methods Mouse embryotic NSCs were isolated and their self-renewal and differentiation were characterized by immunofluorescence. NSCs were exposed to 4.1% sevoflurane 2 h daily for three consecutive days. The potential toxicities of sevoflurane against NSCs were evaluated by neurosphere formation, 5-ethynyl-2'-deoxyuridine (EdU) incorporation and flow cytometry assays. The Peg13, miR-128-3p and Sox13 expression in NSCs were quantified. The potential interactions among Peg13, miR-128-3p and Sox13 were analyzed by luciferase reporter assay. The effects of Peg13 and/or miR-128-3p over-expression on the sevoflurane-related neurotoxicity and Sox13 expression were determined in NSCs. Results The isolated mouse embryotic NSCs displayed potent self-renewal ability and differentiated into neurons, astrocytes and oligodendrocytes in vitro, which were significantly inhibited by sevoflurane exposure. Sevoflurane exposure significantly down-regulated Peg13 and Sox13, but enhanced miR-128-3p expression in NSCs. Transfection with miR-128-3p mimics, but not the control, significantly mitigated the Peg13 or Sox13-regulated luciferase expression in 293T cells. Peg13 over-expression significantly reduced the sevoflurane-related neurotoxicity and increased Sox13 expression in NSCs, which were mitigated by miR-128-3p transfection. Conclusion Such data indicated that Peg13 mitigated the sevoflurane-related neurotoxicity by sponging miR-128-3p to preserve Sox13 expression in NSCs.


2015 ◽  
Vol 6 (1) ◽  
Author(s):  
Steven J Collins ◽  
Carolin Tumpach ◽  
Qiao-Xin Li ◽  
Victoria Lewis ◽  
Timothy M Ryan ◽  
...  

2017 ◽  
Vol 19 (6) ◽  
pp. 372-383 ◽  
Author(s):  
Katari Venkatesh ◽  
L. Vinod Kumar Reddy ◽  
Salar Abbas ◽  
Madhubanti Mullick ◽  
Erfath Thanjeem Begum Moghal ◽  
...  

2017 ◽  
Vol 41 (2) ◽  
pp. 819-834 ◽  
Author(s):  
Tingting Liu ◽  
Xianwei Zeng ◽  
Fangling Sun ◽  
Hongli Hou ◽  
Yunqian Guan ◽  
...  

Background/Aims: EphB4 belongs to the largest family of Eph receptor tyrosine kinases. It contributes to a variety of pathological progresses of cancer malignancy. However, little is known about its role in neural stem cells (NSCs). This study examined whether EphB4 is required for proliferation and differentiation of human embryonic neural stem cells (hNSCs) in vitro. Methods: We up- and down-regulated EphB4 expression in hNSCs using lentiviral over-expression and shRNA knockdown constructs and then investigated the influence of EphB4 on the properties of hNSCs. Results: Our results show that shRNA-mediated EphB4 reduction profoundly impaired hNSCs self-renewal and proliferation. Furthermore, detection of differentiation revealed that knockdown of EphB4 inhibited hNSCs differentiation towards a neuronal lineage and promoted hNSCs differentiation to glial cells. In contrast, EphB4 overexpression promoted hNSCs self-renewal and proliferation, further induced hNSCs differentiation towards a neuronal lineage and inhibited hNSCs differentiation to glial cells. Moreover, we found that EphB4 regulates cell proliferation mediated by the Abl-CyclinD1 pathway. Conclusion: These studies provide strong evidence that fine tuning of EphB4 expression is crucial for the proliferation and neuronal differentiation of hNSCs, suggesting that EphB4 might be an interesting target for overcoming some of the therapeutic limitations of neuronal loss in brain diseases.


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